Lecture 8: Brain Plasticity

Clinical and Experimental Neuropsychology

Developmental Plasticity
sticity is any change in neuronal
nction
tal brains contain 30-60% more
n adult primate brains. Corpus
400% more axons
station there are widespread
n type and location of cells and
rconnections
tion largely ends at birth but
n local cortical connectivity
xposure to particular stimuli
(i.e.

Developmental Plasticity
ct of brain lesions
re age 1 greatest impairment
-5 reorganisation of brain function
+ - little or no sparing of function

The brain was constructed to

change (Merzenich, 2003)
ck of plasticity once the sensitive periods of development
ssed
assumption that the mature brain is hardwired
vances in cognitive ability were ascribed to alterations in
ty between existing neurons
realisation that plasticity still occurs to some degree
rom injury, learning, memory
hood onwards the brain modifies its machinery in a more
way, refinement.
representation of behaviorally relevant input

Exploring Neuroplasticity
ects of Practice
covery from Brain Injury

Sensory and Motor Maps can be

modified with experience
nich et al (1980s) Primate Studies

Pascual-Leone et als (1993)

Braille readers
ed motor cortex for representations of
g finger in Braille readers and controls
rally

Findings
representation of reading finger significantly
at the expense of representation of other
n Braille readers only
n observe changes within a day when Braille
ced for 4-6 hours (Pascual-Leone et al.,

ed with piano players & other learning

nts

Pascual-Leone et al (1995)
ng on a specific piano exercise with one
2 hr/day.
sed motor output maps after 5 days compared
rained hand.
rol group played piano at will for 5 days
rmediate map

Enhanced Representational Fidelity

d, goal-directed practice is key

Experiment asked Ss to practice piano

exercises stead of physically

is doing! Uncovers a fundamental link between

d action

sticity changes are inherently

mpetitive
a result, they are not always
positive

aneous stimulation of 5 fingers

d differentiation in cortical maps

Phantom Limbs
anisation in somatosensory cortex following
ation / denervation
erented cortex becomes functionally
ted by surrounding cortex
m limbs: awareness of a nonexistent body
mentally competent individuals
hs post-op: 90% experience phantom limb
ons, 67% phantom limb pain (Jensen et al,

d sensations on the phantom limb when

nt sites are stimulated
raphical effect: when moving a stimulus
adjacent area, speed, distance & direction
vement are felt in phantom limb

Examples of labile body image

a car extension of body boundaries
of balance following lengthy bus or
urney
mage illusions
er hand illusion

Changing the body image with illusions

sed on the Pinocchio illusion
ckner, 1988) sensation that body
s change size & shape
se illusions make use of the fact that
ration of the skin over the tendon of a
extensor muscle elicits a vivid
esthetic illusion that the joint is
ssively flexing:

Neural Substrate of Body Size: Illusory

Feeling of Shrinking of the Waist
(1988) if vibrated body part touches another body
sensation arises that the touched part changes
e:

Results
vity in the cortices lining the left
central sulcus and the anterior part of the
parietal sulcus reflected the illusion of
st shrinking, and this activity was
lated with the reported degree of
king
gests that altered body images are
mputed by higher-order somatosensory
tal areas, through integration of more
mentary somatic signals

Mechanisms underlying
neuroplasticity
Change in balance of excitation
inhibition - can happen very quickly
ibition is removed, regions of functional
ence are increased

Strengthening of exisiting
ses, e.g. through long-term
ation (LTP)

change in neuronal membrane

xcitability
anatomical changes, e.g. sprouting
new axonal terminals & formation of new
synapses
omical changes take longertraditionally
considered as feasible mechanisms of
icity
chanisms are not mutually exclusive
ic changes occur on multiple time
scales

Hebbian learning
nt framework for bridging neural and
oural levels of analysis
nciple: two neurons or groups of neurons
disconnected may become connected if
re repeatedly activated at the same time
Cells which fire together wire together
rsely, if the firing pattern between
neurons atedly nonsynchronous then the
ction may become inhibited

Cells which fire apart wire apart

Maladaptive connections

in clinical/rehab settings, not all experience

od
me type of stimulation may exaggerate
ts in a vulnerable circuit
mpetitor network may be activated which
er inhibits an already malfunctioning
ork (Kapur, 1996)
during rehab lecture.

Promotion of Adaptive
connections
case scenario: to foster adaptive
ections within a lesioned network and
mise the possiblity of accidently fostering
y connections with other networks.
b et al (1993). Patients suffer
unilateral kes leading to poor function of
one upper
t is the best way to activate the
unctional limb in view of Hebbian

Taubs approach:

scourage patients from using their good limb,

ep hand at rest in pocket.
courage use of dysfunctional limb
ndings: significant improvement in motor
nction after 2 weeks lasting up to two years
, postive effects resulting from a specific pattern
stimulation; activation of one limb combined
th deactivation of the other

Neurogenesis in the adult human

brain?
et al (1998): new cells emerging in caudate
and hippocampus
xperience-dependent: more cell genesis in
n enriched environments than impoverished
t al, 1999)
may reduce occurrence of neurogenesis (e.g.
et al 1999, Vietnam Veterans)

Evidence of Structural Plasticity in Adulthood

e et al. (1997) Experienced taxi drivers found to
larger right hippocampi than novices and
rols.

Negative Plasticity and Cognitive Decline?

point the flipside of this plasticity is that cells
connections may atrophy and die due to lack of
negative plasticity
to keep the mind active into old-age to prevent
tive deterioration like Alzheimers Disease and
ntia
dons Nuns Studies (1996, 1997, 2000)
arch on plasticity shows we remain amenable to
degree of change throughout the lifespan

Cognitive Enrichment offsets Cognitive Decline

Coq and Xerri (2001) Neuroscience

Open questions remain

re the mechanisms and precise principles
functional & structural neuroplasticity ?
versus harmful stimulation?
parts of cortex equally flexible ? What about
ical structures ?
t extent are higher cognitive functions
to experience dependent plasticity?
lisation?

Predictors of recovery?
Age
Sparing of frontal lobes
Awareness of deficit
esion size
Extent of rehabilitation
High IQ

References
d Whishaw, Gazzaniga et al:
Plasticity r
l Merzenich,
mis.com/brainsciencepodcast/2009/02/54-merzenich/

son IH, Murre JJ (1999) Rehabilitation of

amage: Brain Plasticity and Principles of
Recovery. Psychological Bulletin
4-575.
and Cummins (2009). Chapter on Pascualstudy
chandran Phantoms in the brain youtube